Donald P. Dressler

Corticosteroid treatment of experimental smoke inhalation.

The effect of four corticosteroid analogs was evaluated in the treatment of smoke inhalation injury. Rats were exposed to white pine smoke for 15 minutes at 25 C, in a specially designed smoke apparatus. Methylprednisolone, 10 mg bid × 2d, starting one hour post exposure, was most effective in reducing expectant mortality (22.6%). A single injection of methylprednisolone, 20 mg, at one hour, resulted in a 76.7% reduction. There was no significant difference between the single injection of methylprednisolone and dexamethasone, 4 mg, but the administration of analogs with primarily mineraJocorticoid activity, cortisone and hydrocortisone, actually increased mortality. In the control rats, marked interstitial edema occurred by 24 hours, the absence of which following treatment correlated closely with the results of the mortality study. This suggests that post exposure death due to white pine smoke is a result of direct lung injury, with increased endothelial and alveolar membrane permeability and edema, and that administration of glucosteroids in massive doses was effective in reducing this permeability and resultant edema.

Thermal injury and child abuse: the medical evidence dilemma.

The defense of the innocent, as well as the prosecution of the guilty, is a basic premise of American justice. This article reviews nine cases defended by the public defender system, in which the authors were involved, that illustrate some of the pitfalls in making the diagnosis of child abuse and/or neglect caused by thermal injury. The basis for the defense is also discussed, together with the biologic, engineering, and socioeconomic factors. The definition of child abuse and/or neglect is discussed, as is the devastating and long-lasting label of a false accusation, much less false imprisonment. In this regard this review concludes that professionals with thermal injury expertise must become involved in the judicial process if justice is to prevail.

A silicone-nylon laminated dressing (IP-758) for closure of excised or débrided burn wounds.

A synthetic dressing (IP-758) consisting of a silicone membrane with a laminated layer of nylon fabric was evaluated in patients as a substitute for biological materials to cover excised areas of burn wounds. During a 3-day interval, the tissue developed a tightly adherent bond to the synthetic dressing. The IP-758 conformed to irregularly-shaped regions and stretched with the movements of the wound surface. Seventeen burned children from 3 to 12 years of age and 1 adult are included in this study. In 12 cases, the mean area covered with the synthetic ranged from approximately 39 to 118 cm2. The average dressing remained in place for 3 days and was replaced once. Microbiological sampling (wet swab technique) of the area under the IP-758 after application of second dressing was compared with open control sites treated with topical antibiotics. The results with Staphylococcus aureus, a frequent contaminant, were similar for the two test areas. The IP-758 site in 6 patients contained an average of 10 3 S. aureus per swab test. Immediately following removal of the adherent IP-758 and control of local bleeding, the wounds in most patients provided excellent sites for autografts. The IP-758 dressing is well-tolerated, elastic and adherent to the burn wound permitting maturation of the wound to readily accept autografts.

Pulmonary Bacterial Susceptibility in the Burned Rat

An in vivo model system, using the burned rat as a model of altered host resistance, was developed and studied to investigate the lungs ability to handle an aerosolized bacterial insult of either P. aeruginosa or S. aureus. Rates of lung bacterial clearance were correlated with mortality, bacteriologic and histologic results. Susceptibility of the lung to sepsis was shown to be directly related to host resistance and was significantly increased following cutaneous thermal injury. Exposure of burned, non-seeded rats to a bacterial aerosol on day one post burn resulted in a mortality of 50% (P. aeruginosa) and 11.1% (S. aureus). This mortality clearly demonstrates an increased susceptibility at day one post burn. In contrast, this susceptibility gradually decreased with time; no mortality in the burned rat when exposed on day six post burn or in the normal, unburned rat. Histologic findings correlate well with the mortality results showing a gradually decreasing severity of pneumonitis if aerosol exposure was further delayed. Lung bacterial clearance studies revealed that the initial good response of the pulmonary defense mechanisms immediately following aerosol challenge are short-lived and that a marked increase in pulmonary bacterial susceptibility occurs as early as 24 hours following thermal injury.

Eschar: A major factor in postburn pneumonia

Abstract Lung bacterial clearance and mortality studies after a bacterial aerosol challenge together with the determinations of alveolar macrophage function were utilized to assess pulmonary bacterial susceptibility in unburned and burned rats subjected to various grafting procedures. These studies demonstrated that the burned rat is highly susceptible to the development of fatal pneumonitis during the early postburn period. Excision and grafting result in normal bacterial clearance rates and stimulate phagocytosis and intracellular killing by alveolar macrophages present in the lung; however, mortality is not reduced unless an artificial skin is utilized. These studies suggest that burning and grafting result in enhancement of the mechanism by which the lung handles a bacterial challenge but that the effect is short-lived.

Pulmonary bacterial defense: Effect of the burn wound on transfer of alveolar macrophage activation in rats by parabiosis☆

The alveolar macrophage was studied in parabiotic rats using an inbred strain. Parabiotic pairs were sutured together at five weeks of age. Rats were subjected to a full thickness cutaneous burn of 20 per cent of the body surface area at seven weeks of age, and alveolar macrophages were washed from the lungs at six days post burn. The number of alveolar macrophages, their per cent of activation, and their ability to phagocytize and kill P aeruginosa in vitro were significantly increased at six days post burn in the burned controls and in both the burned and unburned members of the parabiotic pairs. No change in the alveolar macrophages was found in either unburned parabiotic pairs or in those which were sham-burned. These results indicate that a humoral or cellular agent produced either within the cutaneous burn wound or elsewhere as a response to the injury, traverses the parabiotic cross circulation to stimulate the alveolar macrophages.